Hi, I've been battling this since 2013, induced by stress.  After trying every kind of topical option, I was approved for Stelara with my insurance in Dec 2015.  After undergoing initial blood tests, I had two TB Gold tests come back "indeterminate".  Both my physician and dermatologist had never seen this before. They are usually either positive or negative, right?   We first thought it was a lab error but after the second one they wanted me to go to an infectious disease specialist.  I could not find one to except me so I put it on hold until the new year....and then I got a cold, then I got a sinus infection, then I got busy, then an event of extreme stress and constant anger causaed an outbreak of Shingles on my forehead! (Ocular nerve from eye to brain was affected. I was 39 years old!).  That virus and the 3,000 mg a day of anti-viral medicine for 10 days knocked me down for a month. Anxiety and anger was replaced with withdrawal, depression and a massive outbreak of psoriasis. Celexa changed my life emotionally,  that's another topic.  I'm so thankful for my physician.  In November 2016 I felt better than I had in over a year, so I decided to start the process of Stelara again. TB Gold negative!  I believe everything happens for a reason. Those two tests that didn't make sense happened because I was not meant to be on this injection yet. I am scared to think of how bad it. I have been if I had been on Stelara during that time. So as we started the process again, in the meantime they gave me Enstilar, luckily at no cost to me, due to a manufacturer incentive and a specialty pharmacy.   Four weeks later I got my first Stelara injection, Dec 1st.  I am anxious to see how well this works!

Side note - Enstilar is AMAZING, short term. On the 2nd day my skin was peeling and feeling very smooth.  On the 4th day the redness went away! On week 3, the week to take a break from it, it  started to come back and spread.  That was the first topical that ever made a difference to me.  I am happy to share a day 4 "before and after" picture if I can figure out how. Ha! 

hello I'm on acetretin 25mg my nails r so brittle does anyone else have this prob. thanks Linda

After a patch of psoriasis has faded, do the white patches that are sometimes left behind fade and disappear over time or do they generally stay?

I have very mild psoriasis and the patches I get are never very big and certainly not very thick yet I've been left with  2-3 small white circles on my arms where I've had psoriasis come and go. Will they disappear?

The odd thing is that I've had stubborn patches disappear after months and not leave any trace they were ever there but then, for example, I had a small patch appear on my right arm about 3 months ago, I applied Dovobet to it for about 3 days and it disappeared and never came back yet it has left a little white patch where it was.

They don't particularly bother me and are certainly preferable to a psoriasis patch but I was just wondering whether they tend to stick around or disappear eventually?

Thanks.

This study shows that Taltz (ixekizumab) gave significant improvements in fingernail psoriasis.

Quote:

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Background:
Fingernail psoriasis is difficult to treat.

Objective:
The objective was to evaluate the effect of ixekizumab, a monoclonal antibody selectively targeting IL-17A, on fingernail psoriasis.

Methods:
This Phase 3, double-blind trial (UNCOVER-3) randomized patients to placebo, etanercept (50-mg twice weekly), or 80 mg ixekizumab as one injection every 4 (IXE Q4W) or 2 weeks (IXE Q2W) after a 160-mg starting dose. At Week 12, ixekizumab patients received open-label IXE Q4W through Week 60; placebo patients received a 160-mg starting ixekizumab dose and etanercept patients a 4-week placebo washout before starting IXE Q4W. Efficacy was assessed by mean per cent Nail Psoriasis Severity Index (NAPSI) improvement at Weeks 12 and 60.

Results:
Of 1346 patients in the UNCOVER-3 trial, this subgroup analysis included only patients with baseline fingernail psoriasis: 116 (60.1%) placebo, 236 (61.8%) etanercept, 228 (59.1%) IXE Q4W and 229 (59.5%) IXE Q2W. At Week 12, greater mean per cent NAPSI improvements were achieved in IXE Q4W (36.7%) and IXE Q2W (35.2%) vs. placebo (−34.3%, P < 0.001 each comparison) and etanercept (20.0%, P = 0.048 vs. Q4W, P = 0.072 vs. Q2W). At Week 60, mean per cent NAPSI improvement was >80% regardless of initial treatment. At Week 12 (nonresponder imputation), complete resolution (NAPSI = 0) was achieved in 19.7% (IXE Q4W), 17.5% (IXE Q2W), 4.3% (placebo, P < 0.001 each comparison) and 10.2% (etanercept, P < 0.05 each comparison) of patients. By Week 60, >50% of patients achieved complete resolution.

Conclusions:
At Week 12, significant improvements in fingernail psoriasis were achieved with ixekizumab therapy. With IXE Q4W maintenance dosing, additional improvement was demonstrated through 60 weeks, and >50% of patients achieved complete resolution.

Hi everyone I am new here, I live in Somerset and have had psoriasis for about 20 years. On Monday I am starting cosentyx. Rather nervous, but excited at the same time.

Has anyone ever had a look at this website?  I found it somewhat informative.  Just posting in case it is helpful to someone.  
I'm having a hard time with the psoriatic arthritis today (if that's really what it is...), damn knee won't stop throbbing.  Might just be old age or a faulty knee, but because my psoriasis is so bad, the doc thinks it MAY be psoriatic arthritis.  Great, now I get to have both!

Anyway, here's the website that a friend forwarded to me today.  I had not seen it myself.  LINK REMOVED  

Of course, the only REAL positive and helpful site of LASTING value, is right here, folks!  Step right in!!!!  (And thanks to all of you that talk and listen and post and reply and help and encourage and make others laugh...)

I don't often have time to get online, but I must admit that I do love THIS site...the psoriasis club!

This study is suggesting that Stelara (ustekinumab) could be aiming at the wrong target. The study from Researchers at the University of Zurich and the Center of Allergy and Environment in Munich suggests that IL-12 could actually be beneficial to patients with psoriasis.

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Abstract:

Neutralization of the common p40-subunit of IL-12/23 in psoriasis patients has led to a breakthrough in the management of moderate to severe disease. Aside from neutralizing IL-23, which is thought to be responsible for the curative effect, anti-p40 therapy also interferes with IL-12 signalling and type 1 immunity.

Here we dissect the individual contribution of these two cytokines to the formation of psoriatic lesions and understand the effect of therapeutic co-targeting of IL-12 and IL-23 in psoriasis.

Using a preclinical model for psoriatic plaque formation we show that IL-12, in contrast to IL-23, has a regulatory function by restraining the invasion of an IL-17-committed γδT (γδT17) cell subset.

We discover that IL-12 receptor signalling in keratinocytes initiates a protective transcriptional programme that limits skin inflammation, suggesting that collateral targeting of IL-12 by anti-p40 monoclonal antibodies is counterproductive in the therapy of psoriasis.

This study looked at the increased risk of cardiovascular (CV) problems in psoriatic arthritis patients.

Quote:

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Objective:
To examine the prevalence and incidence of cardiovascular (CV) risk factors, including hypertension, hyperlipidemia, diabetes mellitus (DM), and obesity among patients with psoriatic arthritis (PsA) and rheumatoid arthritis (RA) compared to the general population, and to examine the treatment of incident CV risk factors in PsA and RA compared to controls.

Methods:
A cohort study was conducted within The Health Improvement Network, a medical record database in the UK, using data from 1994 to 2014. Patients ages 18–89 years with PsA or RA were matched to controls on practice and start date. The prevalence and incidence of CV risk factors identified by diagnostic codes were calculated. Cox proportional hazards models were used to examine the relative incidence of these CV risk factors. Finally, pharmacologic therapies for incident CV risk factors were examined.

Results:
Study subjects included patients with PsA (n = 12,548), RA (n = 53,215), and controls (n = 389,269). The prevalence of all CV risk factors was significantly elevated in PsA. Only the prevalence of DM and obesity was increased in RA. Incidence of hypertension, hyperlipidemia, and DM was elevated in PsA and RA. Receipt of therapy within 1 year following incident diagnosis of CV risk factors was not substantially different between the groups; approximately 85%, 65%, and 45% of patients received prescriptions for hypertension, hyperlipidemia, and DM, respectively.

Conclusion:
Patients with PsA have an increased prevalence of CV risk factors, and both patients with PsA and patients with RA have increased incidence of a new diagnosis of CV risk factors. Pharmacologic treatment of CV risk factors in patients with PsA and RA was similar to controls in the UK.

This study looks at how well medication is used in the long-term topical treatment of psoriasis.

Quote:

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Background:
Most people with psoriasis have limited disease that could be treated with topicals, but topical efficacy is limited by low short-term adherence. Psoriasis is a chronic disease, and long-term adherence is an even bigger problem.

Objectives:
To determine how well medication is used in the long-term topical treatment of psoriasis and to assess the potential of an internet-based reporting intervention to improve treatment adherence and outcomes.

Methods:
An investigator-blinded, prospective study evaluated topical fluocinonide adherence in 40 patients with mild-to-moderate psoriasis over 12 months. Subjects were randomized in a 1 : 1 ratio to standard-of-care or internet-based reporting group. Adherence was objectively monitored with Medication Event Monitoring System® caps.

Results:
Fifty per cent of subjects discontinued the treatment. Greater adherence was seen in the intervention group compared with the standard-of-care group (50% vs. 35%, P = 0·08). Psoriasis Area and Severity Index improved more in the intervention group at month 1 (1·61 vs. −0·12, P = 0·003), month 3 (2·50 vs. 0·79, P = 0·025) and month 12 (3·32 vs. 0·34, P = 0·038) than in the standard-of-care group.

Conclusions:
This study likely underestimates the challenge of long-term adherence, as adherence tends to be better in research studies than in clinical practice. This study also did not fully account for primary nonadherence. Adherence to topical treatment is low in the short term and decreased further in the long term, a considerable challenge for dermatologists to address. A reporting intervention may be one of the ways we can improve our patients’ treatment outcomes.

This study suggests CXCL10 could be a predictive biomarker for the onset of psoriatic arthritis.

Quote:

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Objective:
Biomarkers that can predict the development of psoriatic arthritis (PsA) in patients with psoriasis would be useful in clinical practice. The aim of this study was to assess whether CXCL10 could be a predictive biomarker of PsA prior to its onset.

Methods:
Psoriasis patients without arthritis were followed up prospectively and assessed annually for development of PsA by a rheumatologist. Patients in whom PsA developed were designated as converters, while those in whom PsA did not develop were termed nonconverters. Baseline serum concentrations of CXCL10 were measured by Luminex assay in 46 converters and 45 nonconverters.

Results:
The level of CXCL10 was significantly higher in converters (median 493 pg/ml [interquartile range (IQR) 356–984]) than in nonconverters (median 371 pg/ml [IQR 263–578]; P = 0.005). In contrast, C-reactive protein (CRP) levels were not significantly different between converters and nonconverters at baseline. CXCL10 was associated with conversion status after adjustment for age, sex, duration of psoriasis, and duration of follow-up (odds ratio 1.3, 95% confidence interval 1.1–1.5, P = 0.004). In a subset of converters, the CXCL10 level was significantly higher at baseline (median 927.4 pg/ml [IQR 547.6–1,243]) than after PsA diagnosis (491.5 pg/ml [IQR 323.2–607]; P < 0.0001), while CRP levels were lower at baseline (26.6 μg/ml [IQR 16.37–62.75]) than after PsA diagnosis (36.1 μg/ml [IQR 14.74–101.7]; P = 0.003). CXCL10 gene expression was increased 17.3-fold in synovial fluid (SF) compared with blood from PsA patients (P = 0.01) and 44.3-fold in the SF of PsA patients compared with the SF of patients with gout (P = 0.001).

Conclusion:
CXCL10 may be involved in PsA pathogenesis and is a candidate predictive biomarker for PsA in patients with psoriasis.

Celgene have said Otezla met it's primary endpoint in patients with psoriatic arthritis.

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Celgene Corporation today announced findings from the ACTIVE phase 3b clinical trial of OTEZLA® (apremilast), the Company's oral, selective inhibitor of phosphodiesterase 4 (PDE4), at the 2016 American College of Rheumatology/Association of Rheumatology Health Professionals (ACR/ARHP) Annual Meeting in Washington, D.C. The trial met its primary endpoint of significant improvement in the proportion of patients achieving an ACR20 response at week 16 with OTEZLA versus placebo in patients with active psoriatic arthritis who have not previously been treated with a biologic therapy.

The ACTIVE trial randomized 219 patients who may have had one prior conventional therapy and were not previously treated with a biologic to either OTEZLA 30 mg twice daily (n=110) or placebo (n=109). An objective of the study was to determine the clinical effects of OTEZLA compared with placebo, by examining efficacy outcomes at earlier time points than in previous studies.

"These findings show a separation from placebo as early as two weeks with oral OTEZLA in patients with psoriatic arthritis who have not been previously treated with biologics," said Dr. Jacob Aelion, director of the West Tennessee Research Institute and clinical professor of Medicine/Rheumatology at the University of Tennessee in Memphis. "Early responses at week 2 across several measures of disease activity, including morning stiffness and enthesitis, were also seen at week 16."

A separation between OTEZLA and placebo was seen at week 2, the study's first efficacy assessment time point, with 16.4 percent of patients in the OTEZLA arm achieving ACR20, compared with 6.4 percent in the placebo arm. Improvements versus placebo were also seen at week 2 in 28-joint count Disease Activity Score (C-reactive protein) [−0.59 vs. −0.31, respectively], health assessment questionnaire disability index (HAQ-DI) [−0.13 vs. −0.05], morning stiffness severity [42.7 percent vs. 21.1 percent], and enthesitis (inflammation at sites where tendons or ligaments insert into bone), as measured by a change in Gladman Enthesitis Index (GEI) [−1.1 vs. −0.4]. A trend to decrease in swollen joint count was also observed in patients receiving OTEZLA compared with those on placebo (−27.7 percent for OTEZLA vs. −17.5 percent for placebo).

At week 16, 38.2 percent of patients in the OTEZLA arm achieved an ACR20 response, compared with 20.2 percent in the placebo arm. Improvements were also seen at week 16 in other measures of disease, including: 28-joint count Disease Activity Score (C-reactive protein) (−1.07 with OTEZLA vs. −0.39 with placebo), swollen joint count (−46.4 percent vs. 4.2 percent, respectively), HAQ-DI (−0.21 vs. −0.06), improvement in morning stiffness severity (46.4 percent vs. 25.7 percent), and enthesitis (−1.5 vs. −0.4).

At week 24, placebo patients crossed over to active treatment with OTEZLA. Responses demonstrated in the placebo-controlled phase were maintained through week 52. For patients who were on OTEZLA from baseline, ACR20, ACR50, and ACR70 response rates at week 52 were 67.1 percent, 36.7 percent and 21.3 percent, respectively, and observed percent change in swollen joint count was −77.5 percent. Among patients who had enthesitis at baseline, GEI of 0 was 69.8 percent.

The most commonly reported adverse events during the placebo-controlled period were nasopharyngitis (8.3 percent with OTEZLA vs. 6.4 percent with placebo), nausea (8.3 percent vs. 1.8 percent, respectively), headache (7.3 percent vs. 3.7 percent), hypertension (6.4 percent vs. 6.4 percent), diarrhea (14.7 percent vs. 11.0 percent) and upper respiratory tract infection (4.6 percent vs. 10.1 percent). Serious adverse events in the OTEZLA and placebo arms were 2.8 percent and 4.6 percent, respectively. No increase in adverse event incidence or severity was seen through week 52.

Hi all, Dave from Melbourne here. 
I was first diagnosed in 1978 with plaque psoriasis. It has come and gone over the years and until recently it has been the worst ever. Just turned 51.  It is hereditary in my family and was originally. My Father had it and 1 of my brothers has it but  only the one that affects the nail beds. 

Anyway I was introduced to a triangle of products 2 weeks ago and I am over the moon. It is starting to recede and not be as angry or itchy. Have had the Voluptuous itching for as long as can remember but have not had an episode for over a week now. 

I
Am so stoked right now. 
Cheers, and thanks for reading.

Well I started my first injection on Tuesday for Cosentyx and I have to say my psoriasis is already disappearing and its only been 6 days.  I am really excited and being optimistic, I will keep everyone updated on my progress.

Nick

Even the snows of New Hampshire don't stop psoriasis...

My acquaintance with psoriasis began in 1992.  I have numerous mild plaques that seem almost stable, due to medication, or perhaps in spite of medication.  The medics like to prescribe Taclonex and Cordran tape.  The tape has been effective, but I use it very sparingly.  Taclonex, even generic, is shamefully expensive.  Its Calcipotriene component is the expensive one, at 10$/gram.

Let me extend sympathy to those with severe psoriasis.  Courage!

This study albeit small shows effectiveness and tolerability of Stelara in treating palmoplantar pustular psoriasis.

Quote:

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Background:
Palmoplantar pustular psoriasis is a chronic inflammatory skin disease that is associated with considerable impairment in quality of life and resilience. Given the lack of approved pharmacological agents for this indication and the frequently recalcitrant disease course, therapeutic options are limited.

Patients and methods:
Following unsatisfactory therapeutic attempts with other treatment modalities, nine patients (six women; three men) were treated with ustekinumab (45 mg in individuals < 100 kg body weight, 90 mg in individuals > 100 kg) at weeks 0, 4, 12, and 24. Latent tuberculosis was ruled out prior to treatment. Regular follow-up was done at week 4 and 12, and every 12 weeks thereafter.

Results:
Average age at the beginning of treatment was 48 years. Four patients achieved 75 % improvement in the palmoplantar Psoriasis Area Severity Index (PASI). Overall, there was an average improvement in the palmoplantar PASI of 71.6 % after 24 weeks. Two patients exhibited complete resolution after 24 weeks. Besides local injection site reactions and mild infections, no adverse effects were observed.

Conclusions:
This case series provides further evidence for the effectiveness and tolerability of ustekinumab in the treatment of palmoplantar pustular psoriasis. Controlled studies and observations in the context of patient registries are required to assess long-term efficacy and safety as well as the potential therapeutic benefit of intermittent therapy.

This study looked at drug survival rates of systemic treatments in psoriasis patients.

Treatments involved:
Fumaric acid esters (FAE)
Methotrexate (MTX)
Acitretin (ACI)
Cyclosporine A (CyA)
Adalimumab (ADA)
Etanercept (ETA)
Infliximab (INF)
Ustekinumab (UST)

Quote:

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Background and objectives:
Moderate-to-severe psoriasis frequently requires long-term systemic therapy. Reflecting efficacy, safety, and treatment satisfaction, drug survival is an indicator of therapeutic success. The objective of the present study was to assess drug survival rates and reasons for discontinuation of fumaric acid esters (FAE), methotrexate (MTX), acitretin (ACI), cyclosporine A (CyA), adalimumab (ADA), etanercept (ETA), infliximab (INF), and ustekinumab (UST) in patients with moderate-to-severe psoriasis.

Patients and methods:
We performed a retrospective analysis of 373 patients who had received a total of 696 treatment courses at a German university hospital in the period 1/2003–5/2014.

Results:
The crude probability of survival was highest for UST, followed by ADA, ETA, INF, FAE, MTX, ACI, and CyA. In multivariate regression analysis using FAE as reference, hazard ratios (HR) for discontinuation were 0.14 (95 % confidence interval: 0.06–0.35) for UST, 0.43 (0.26–0.73) for ADA, 2.11 (1.14–3.91) for ACI, and 3.26 (1.44–7.39) for CyA. INF showed longer survival when combined with MTX (HR 2.87, 1.21–6.81). Traditional systemic antipsoriatic agents as well as INF were most frequently discontinued due to adverse events; all other biologics, due to inefficacy with respect to cutaneous lesions.

Conclusions:
Drug survival rates should be integrated into therapeutic decisions in order to provide patients with an optimal long-term strategy.

This study compared 4 bio treatments for scalp psoriasis. The bio's in the study were:
Remicade (infliximab)
Enbrel (etanercept)
Humira (adalimumab)
Stelara (ustekinumab)

Quote:

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Background:
The scalp is a frequent and difficult-to-treat localization of psoriasis. Little evidence exists regarding the use of biologic agents in recalcitrant cases of scalp psoriasis that are resistant to other treatment options.

Objectives:
To evaluate and compare the efficacy of currently available biologic agents (infliximab, etanercept, adalimumab, ustekinumab) in the treatment of scalp symptoms in patients suffering from moderate to severe plaque psoriasis.

Materials and methods:
This retrospective cohort study consisted of a review of the database of all psoriasis patients who suffered from scalp symptoms and received biologic treatment between January 2012 and December 2014. The patients were divided into four groups based on the drug administered. Scalp psoriasis severity was assessed by the Psoriasis Scalp Severity Index (PSSI) at baseline and at weeks 4, 12, 24 and 48. Psoriasis severity was evaluated with the Psoriasis Area and Severity Index (PASI) at the same time points.

Results:
In total, 145 patients were enroled in the study (infliximab n = 35, etanercept n = 30, adalimumab n = 39, ustekinumab n = 41). At week 4, the infliximab group achieved a 74% mean decrease in the PSSI (ΔPSSI), followed by mean decreases of 61.7%, 53.1% and 53.7% in the ustekinumab, etanercept and adalimumab groups respectively. The differences in the ΔPSSI were lower at week 48: ustekinumab 94.9%, infliximab 94.3%, etanercept 83.1% and adalimumab 89.0%. The PASI score improved sufficiently in all treatment groups. Infliximab and ustekinumab exhibited greater efficacy at weeks 4 and 12. This difference was not as prominent as that revealed by the PSSI. At week 48, the differences in the ΔPASI were barely statistically significant (P = 0.048).

Conclusions:
All four biologic agents yielded significant improvement in both scalp and skin lesions. Ustekinumab and infliximab exhibited the greatest efficacy, which was clinically meaningful from the early stages of the study. Adalimumab and etanercept followed, yielding satisfactory improvement rates.

This study investigated the immunogenicity of Cosentyx (secukinumab) across six phase III clinical trials in patients with plaque psoriasis were treated with for up to 52 weeks and additionally followed up at week 60.

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Background:
The proinflammatory cytokine interleukin (IL)-17A plays a pivotal role in psoriasis pathogenesis. Secukinumab, a fully human monoclonal antibody (mAb) that selectively targets IL-17A, has been demonstrated to be highly efficacious for the treatment of moderate-to-severe psoriasis, starting at early time points, with a sustained effect and a favourable safety profile. mAb therapies may be associated with production of antidrug antibodies (ADAs) that can affect drug pharmacokinetics, diminish response or cause hypersensitivity reactions.

Objectives:
To investigate the immunogenicity of secukinumab across six phase III clinical trials in which patients with plaque psoriasis were treated with secukinumab for up to 52 weeks and additionally followed up at week 60.

Methods:
Immunogenicity in patients with plaque psoriasis exposed to secukinumab was evaluated at baseline and at weeks 12, 24, 52 and 60. Treatment-emergent (TE)-ADAs were defined as a positive ADA signal detected in post-treatment samples from patients with a negative baseline signal. Confirmed positive samples were further analysed for their drug-neutralizing potential.

Results:
Among 2842 patients receiving secukinumab and evaluated for ADAs, 11 (0·4%) developed TE-ADAs. Associations between TE-ADAs and secukinumab dose, frequency or mode of administration were not observed. Neutralizing antibodies were detected in three of nine evaluable patients with TE-ADAs.

Conclusions:
Secukinumab immunogenicity was low, as shown by TE-ADA detection in only 11 of 2842 (0·4%) patients with moderate-to-severe plaque psoriasis treated with secukinumab. All but one of the patients with TE-ADAs were biologic naive. Neither TE-ADAs nor neutralizing antibodies were associated with loss of secukinumab efficacy or issues of clinical concern.

This study was to evaluate the prevalence and clinical aspects of and the risk factors for nail involvement in French children with psoriasis.

Quote:

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Background/Objectives:
Little information is available on the prevalence and clinical aspects of nail involvement in children with psoriasis. The objective of this study was to evaluate the prevalence and clinical aspects of and the risk factors for nail involvement in French children with psoriasis.

Methods:
We performed a multicenter, cross-sectional study in 23 French dermatology centers. All children seen during the 1-year study were systematically included. Clinical features of the nails were collected. Association with clinical aspects of the disease and comorbidities were evaluated.

Results:
Of 313 children with psoriasis (mean age 9.1 ± 4.2 yrs; 149 boys, 164 girls), 31.1% had familial psoriasis and 30% had severe psoriasis. The mean age at onset was 6.1 ± 3.7 years. Nails were involved in 32.3% of children. The main clinical aspects were pitting (69.1%) for fingernails and onycholysis (40.0%) and pachyonychia (27.5%) for toenails. All of the fingers were involved at similar frequencies, whereas the big toe was involved twice as often as the others (p < 0.005). Nail involvement was associated with male sex (p < 0.001), palmoplantar psoriatic (p < 0.001), severity of disease (p = 0.003), and psoriatic arthritis (p = 0.03).

Conclusion:
The prevalence of nail involvement was 32.3% in children with psoriasis. Clinical aspects in children are reported, as well as clinical associations. As in adults, nail psoriasis is closely associated with psoriatic arthritis.

I miss the Dovonex scalp lotion. Also just regular Dovonex cream. Has anyone tried getting a compounding pharmacy to make up any Dovonex without the steroids?